Ariel M, Adolph A R
J Neurophysiol. 1985 Nov;54(5):1123-43. doi: 10.1152/jn.1985.54.5.1123.
Synaptic drugs were superfused into turtle eyecup preparation while recording extracellularly from directionally sensitive (DS) retinal ganglion cells. As in previous experiments in intact rabbit retina, both picrotoxin (a GABA antagonist) and physostigmine [an acetylcholine (ACh) potentiator] reduced or eliminated the directional selectivity of these cells. These drug effects occurred at micromolar concentrations and were long lasting. Superfusion of ACh caused excitation, and GABA caused inhibition of the spike activity of these DS cells. In some experiments, the ganglion cell was isolated from its presynaptic inputs by perfusing with a low-Ca2+/EGTA perfusate, which blocked synaptic transmission but did not suppress spike firing. During this synaptic block, ACh still caused spontaneous spike firing, and GABA was able to suppress the ACh-induced spike activity. Strychnine slightly increased the spontaneous activity of DS ganglion cells and reduced their response to light. Glycine and taurine were equally effective in totally suppressing spike activity, and strychnine blocked this inhibition by both agents. However, these inhibitory effects may be transynaptic because glycine did not suppress ACh-induced excitation during synaptic block. Superfusion of micromolar concentrations of methionine enkephalin and [D-Ala2]methionine enkephalinamide occasionally caused small increases in the light responses of DS cells, whereas naloxone, a broad-spectrum opiate antagonist, moderately decreased light responsiveness. Because naloxone had no effect on these cell's directional tuning, the opiate system is probably not involved in the mechanism of directional sensitivity. Based on the effects of these transmitter candidates and their antagonists, a possible site fo DS subunits may be the ACh and GABA receptors on the membrane of DS ganglion cells. ACh provides light-evoked excitation that may, when potentiated by physostigmine, overcome asymmetric GABA inhibition. Although the role of glycine in directional sensitivity is small, it may be responsible for regulating presynaptic excitatory pathways leading to the DS ganglion cells.
将突触药物灌流到乌龟眼杯标本中,同时从方向敏感(DS)视网膜神经节细胞进行细胞外记录。与之前在完整兔视网膜上的实验一样,印防己毒素(一种GABA拮抗剂)和毒扁豆碱[一种乙酰胆碱(ACh)增强剂]均可降低或消除这些细胞的方向选择性。这些药物效应在微摩尔浓度下出现且持续时间长。灌流ACh引起兴奋,而GABA则抑制这些DS细胞的动作电位活动。在一些实验中,通过用低钙/乙二醇双四乙酸灌流液灌流,将神经节细胞与它的突触前输入隔离开来,这阻断了突触传递但没有抑制动作电位发放。在这种突触阻断期间,ACh仍然引起自发动作电位发放,而GABA能够抑制ACh诱导的动作电位活动。士的宁略微增加了DS神经节细胞的自发活动,并降低了它们对光的反应。甘氨酸和牛磺酸在完全抑制动作电位活动方面同样有效,而士的宁阻断了这两种物质的抑制作用。然而,这些抑制作用可能是跨突触的,因为在突触阻断期间甘氨酸并没有抑制ACh诱导的兴奋。灌流微摩尔浓度的甲硫氨酸脑啡肽和[D - Ala2]甲硫氨酸脑啡肽酰胺偶尔会使DS细胞的光反应略有增加,而广谱阿片拮抗剂纳洛酮则适度降低光反应性。由于纳洛酮对这些细胞的方向调谐没有影响,阿片系统可能不参与方向敏感性机制。基于这些候选递质及其拮抗剂的作用,DS亚基的一个可能位点可能是DS神经节细胞膜上的ACh和GABA受体。ACh提供光诱发的兴奋,当被毒扁豆碱增强时,可能克服不对称的GABA抑制。尽管甘氨酸在方向敏感性中的作用较小,但它可能负责调节通向DS神经节细胞的突触前兴奋性通路。